CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration.

CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Abstract Text:

Robert D Loberg,Chi Ying,Matt Craig,Li Yan,Linda A Snyder,Kenneth J Pienta,

The ability of CCL2 to influence prostate cancer tumorigenesis and metastasis may occur through two distinct mechanisms: 1) a direct effect on tumor cell growth and function, and 2) an indirect effect on the tumor microenvironment by the regulation of macrophage mobilization and infiltration into the tumor bed. We have previously demonstrated that CCL2 exerts a direct effect on prostate cancer epithelial cells by the regulation of their growth, invasion, and migration, resulting in enhanced tumorigenesis and metastasis. Here we describe an indirect effect of CCL2 on prostate cancer growth and metastasis by regulating monocyte/macrophage infiltration into the tumor microenvironment and by stimulating a phenotypic change within these immune cells to promote tumor growth (tumor-associated macrophages). VCaP prostate cancer cells were subcutaneously injected in male SCID mice and monitored for tumor volume, CD68(+) macrophage infiltration, and microvascular density. Systemic administration of anti-CCL2 neutralizing antibodies (CNTO888 and C1142) significantly retarded tumor growth and attenuated CD68(+) macrophage infiltration, which was accompanied by a significant decrease in microvascular density. These data suggest that CCL2 contributes to prostate cancer growth through the regulation of macrophage infiltration and enhanced angiogenesis within the tumor.

CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Publishing Authors By Initials

RD Loberg,C Ying,M Craig,L Yan,LA Snyder,KJ Pienta,

For similar xenograft model antitumor assays research abstracts see: xenograft model antitumor assays research

PUBMED ID PMID:

MEDLINE DATE:

CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Neoplasia (New York, N.Y.)

VOLUME: 9

Page Numbers: 556-62

Journal Abbreviation: Neoplasia

ISSN: 1476-5586

DAY: 3

MONTH: Jul

YEAR: 2007

CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100886622

CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Keywords Mesh Terms:

KEYWORDS: Xenograft Model Antitumor Assays

MESH TERMS: pathology

Chemical & Substance for Abstract: CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Information

Substance Name: Chemokine CCL2

Registry Number: 0

Grant and Affiliation Information for CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration.

AFFILIATION: Department of Urology, University of Michigan Urology Center, Ann Arbor, MI 48109-0946, USA. rloberg@umich.edu

Country: Canada

AGENCY: United States NCI

GRANT: P50 CA69568-06A

ACRONYM: CA

MEDLINETA: Neoplasia

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration Related Publications

• CCL2 Protects Prostate Cancer PC3 Cells from Autophagic Death via Phosphatidylinositol 3-Kinase/AKT-dependent Survivin Up-regulation.
• CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration.
• CCL2, survivin and autophagy: New links with implications in human cancer.
• In Vivo Evaluation of AT-101 (R-(-)-Gossypol Acetic Acid) in Androgen-Independent Growth of VCaP Prostate Cancer Cells in Combination with Surgical Castration.
• Modeling signal transduction in normal and cancer cells using complex adaptive systems.
• Novel surface expression of reticulocalbin 1 on bone endothelial cells and human prostate cancer cells is regulated by TNF-alpha.
• PAR1-mediated RhoA activation facilitates CCL2-induced chemotaxis in PC-3 cells.
• Rationale for the Radiation Therapy Oncology Group Study RTOG P-0014.
• Rationale for the Radiation Therapy Oncology Group Study RTOG P-0014.
• Simulating the hallmarks of cancer.
• The evolving biology and treatment of prostate cancer.
• The lethal phenotype of cancer: the molecular basis of death due to malignancy.